COVID-19, Inflammation and HPA axis activity, and Risk for Psychopathology in Youth

一场史无前例的精神健康危机和自杀念头和行为(STB)激增 在这一大流行之前并因此而进一步恶化的年轻人中的这种情况。研究表明，年轻人正处于 新冠肺炎感染后1-6个月因精神诊断而接受事件治疗的风险增加。风险： 性传播疾病在感染患者中也会增加；新冠肺炎导致的认知障碍 报告甚至在感染后约4个月。除了发病率和死亡率的增加外，缓解 为减少传播所做的努力给儿童和家庭带来了额外的压力(例如，父母 失业、父母死亡、在线教育)，这些都与精神病发病率的增加有关 在年轻的时候。然而，我们对新冠肺炎感染对人类健康的独特贡献了解有限。 青年精神病理学的发病率和与风险有关的生物机制。不符合法规中的 免疫反应，特别是IL-6、IL-1b、C-反应蛋白(CRP)和肿瘤坏死因子-a及其mRNA的增加 和低皮质醇是新冠肺炎严重程度和精神病理学中常见的生物学机制。 我们的目标是检查新冠肺炎感染对青年精神病理学发病率的影响；它的影响 炎症和HPA轴标记物；并确定临床、认知、生物学和心理社会 有助于预测新冠肺炎感染后发生精神病理的风险的青年的特征。我们 建议招募12-17岁，无精神障碍或慢性病或慢性病病史的青年 感染者：1)最近一个月内感染新冠肺炎(冠状病毒感染者，n=200)；2)无 新冠肺炎、流感或过去6个月内的任何呼吸道感染(非冠状病毒感染，n=200)；3)青年 在过去一个月内有IFV(IFV，n=100)。IFV小组将允许我们检查新冠肺炎或 一般来说，感染与风险有关。参与者将在基线后3、6和18个月进行跟踪 并对精神和身体症状、认知功能、事件精神病理学进行评估；大流行 和非大流行应激源；以及所有时间点的风险和保护因素。在基线、3个月和6个月，我们 将测量炎症(细胞因子、炎症基因的信使核糖核酸)；并收集急性和慢性HPA轴 活动测量(头发皮质醇浓度、唾液皮质醇)。我们假设COVID小组将会显示 精神病理，特别是抑郁症和焦虑症以及性传播疾病的发病风险增加 无COVID组和体外受精组。他们还会表现出更多的炎症以及精神和身体上的反应 症状随着时间的推移；以及HPA轴活动和认知功能随着时间的推移而降低；这些反过来将预测 精神病态的发作。这项研究将增进我们对新冠肺炎感染对人类健康影响的理解 青年精神病理学的风险以及与风险有关的生物机制。结果也将扩大 其他类型的感染。这项研究对于我们为未来的流行病和 大流行，这是不可避免的，而且还在上升。

There has been an unprecedented mental health crisis and a surge in suicidal thoughts and behaviors (STBs) among youth that predated and was further exacerbated by the pandemic. Studies show that youth are at increased risk for incident treatment for psychiatric diagnosis 1-6 months following COVID-19 infection. Risk for STBs is also increased among individuals with infections; and cognitive impairment following COVID-19 is reported even ~4 months following infection. In addition to the increased morbidity and mortality, the mitigation efforts put in place to reduce transmission resulted in additional stressors on children and families (e.g., parental job loss, parental death, online schooling) and these were associated with increased rates of psychopathology in youth. However, we have a limited understanding of the unique contribution of COVID-19 infection on incidence of psychopathology in youth and the biological mechanisms implicated in risk. Dysregulations in immune responses, specifically, increased IL-6, IL-1b, C-Reactive Protein (CRP), and TNF-a and their mRNA and low cortisol are common biological mechanisms implicated in COVID-19 severity and in psychopathology. Our goals are to examine the impact of COVID-19 infection on incidence of psychopathology in youth; its impact on inflammation and HPA axis markers; and to identify clinical, cognitive, biological, and psychosocial characteristics that will help predict youth at risk for onset of psychopathology following COVID-19 infection. We propose to recruit youth, aged 12-17 years, without history of psychiatric disorders or chronic Illness or chronic infections who were: 1) infected with COVID-19 within the past month (COVID, n=200); 2) without history of COVID-19, influenza (IFV), or any respiratory infections in the past 6 months (no-COVID, n=200); and 3) youth with IFV within the past month (IFV, n=100). The IFV group will allow us to examine whether COVID-19 or infections in general are associated with risk. Participants will be followed at 3, 6, and 18 months after baseline and assessed on psychiatric and physical symptoms, cognitive function, incident psychopathology; pandemic and non-pandemic stressors; and risk and protective factors at all timepoints. At baseline, 3, and 6 months, we will measure inflammation (cytokines, mRNA for inflammatory genes); and collect acute and chronic HPA axis activity measures (hair cortisol concentrations, salivary cortisol). We hypothesize that the COVID group will show increased risk of onset of psychopathology, specifically depression and anxiety disorders and STBs, compared to the no-COVID and IVF groups. They will also show increased inflammation and psychiatric and physical symptoms over time; and reduced HPA axis activity and cognitive function over time; and these will in turn predict onset of psychopathology. This study will advance our understanding of the impact of COVID-19 infection on risk for psychopathology in youth and the biological mechanisms implicated in risk. The results will also extend to other types of infections. This study is essential to inform our preparedness efforts for future epidemics and pandemics, which are inevitable and on the rise.